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The population of breast cancer cells that are responsible for cancer recurrence and apoptosis resistance is known as Aim Triple negative breast cancer cells. However, a potential role of CL as a p53- and survivin modulating agent in TNBC cells has not been investigated. Methods MDAMB-231 cells were treated with different concentrations of CL, including viability, p53 gene expression, surviving protein expression, and caspase-3 protein expression were all tested. An increase in caspase-3 expression levels was followed by a 94. 60 - 21. 6 percent decrease in survivin protein levels. CL's remarkably high gene expression ratio increased to 5-fold at 13 u03bcg/mL. As molecular targets of CL contribute to caspase-3-dependent apoptosis in TNBC cells, this compound is an effective p53- and survivin modulating agent in TNBC.
Source link: https://europepmc.org/article/MED/35924809
Therapeutic agents that help re-establish the normal functions of apoptotic signaling pathways are an effective treatment of breast cancer. Active targeting delivery systems were developed for targeting tumor environment and selective cell killing effects in order to enhance its therapeutic efficiency and investigate the mechanism of actions. Cell experiments were carried out to determine the targeted anti-breast cancer effects of FA-BSANPs/BA and its mechanisms. Cellular uptake and MTT showed that it improved targeted uptake effectiveness and cytotoxicity. It is believed that FA-BSANPs/BA's pro-apoptotic mechanism is linked to the control of key proteins in extrinsic apoptotic pathways. In conclusion, FA-BSANPs/BA is a good delivery carrier and significantly reduces breast cancer incidence in comparison to free BA. The reason for FA-BSANPs/BA's success in promoting apoptosis of breast cancer may have been to the caspase-8/Bid/ROS pathway.
Source link: https://europepmc.org/article/MED/34330116
Due to their ability to kill cancer cells that are resistant to platinum-based compounds, gold-based anticancer drugs have piqued increasing academic interest. In addition, apoptosis, caspase 3/7 production, and cell cycle analysis were also carried out to see the effect and mechanism of killing breast cancer cells by the chosen gold I compound, Ph 3 PAu[SC=NC 6 F-3]. The gold compound, Ph 3 PAu[SC=NC 6 F-3], demonstrated low toxicity to H9c2 normal cells, primary breast cancer cells, and breast cancer stem cells, according to MDA-MB-231 and MCF-7 cells, primary breast cancer cells, and breast cancer stem cells. The IC 50 doses of gold compound Ph 3 PAu[SC=NC 6 F-3] against the breast cancer cell lines MDA-MB-231 and MCF-7 were approximately 6-fold lower than that of cisplatin.
Source link: https://europepmc.org/article/MED/35910309
It is important to find novel biomarkers for cervical cancer therapy. Methods HeLa and SiHa were constructed in the current study and presented by puromycin for cervical cell lines HeLa and SiHa with kin17 knockdown, which were transfected with the recombinant lentiviral vector carrying KIN17 siRNA and screened by puromycin. HeLa and SiHa cells infected with gene silencing vectors had high fluorescent positive rates and high gene silencing capacity, according to the results. A total of 5 genes were identified for this risk score, including KIN-related prognostic genes in cervical cancer, but the results revealed that CTLA4 expressions were positively correlated with the risk score. Conclusion Our results showed that kin17 knockdown promotes cervical cancer cell apoptosis by targeting caspase 3, PARP, and Bcl-2 family proteins. In addition, kin17 could reduce cancer cell apoptosis through the mitochondrial pathway, and it could be used as a novel therapeutic target for cervical cancer cell apoptosis regulation.
Source link: https://europepmc.org/article/MED/35909901
BMP signaling in lung cancer cells suppresses AMP activated kinase by inhibiting LKB1. Activated AMPK can promote cancer cell survival, but cell death is triggered by cell death. Methods This paper explores the synergistic effects of two BMP inhibitors along with mitochondrial targeting agents phenformin and Ym155 on lung cancer cells expressing LKB1, LKB1 null, and A549 cells transfected with LKB1, LKB1 null. BMP inhibitors in lung cancer cells expressing LKB1 were enhanced by the combination of BMP inhibitors and mitochondrial targeting agents, which culminated in the activation of AMPK in lung cancer cells expressing LKB1. Cell death in both H1299 and A549 cells was caused by AMPK activation by A769662. In primary NSCLC, combination therapy also increased cell death and AIF nuclear localization. AIF caspase-independence cell death is an evolutionarily conserved cell death pathway that is not often studied in cancer. These studies provide new insight into how cells inducing AIF caspase-independent cell death in cancer cells using BMP inhibitors.
Source link: https://europepmc.org/article/MED/35761398
In the human bladder cancer cell line 5637, the anti-cancer effects of -gingerol, the key active polyphenol of ginger, were investigated. -GIN also raised the intracellular reactive oxygen species levels and TG100-115 or tranilast, respectively, and -GIN increased cell death in U2011-induced cell death. These results show that -GIN activated apoptosis in the bladder cancer cell line 5637 and has the potential to be used in the development of new drugs for bladder cancer treatment.
Source link: https://europepmc.org/article/MED/35919815
Two new families of dithiocarbamate gold complexes derived from benzenesulfonamide, phosphine or carbene as ancillary ligands have been synthesized and described. We found that the more lipophilic complexes, as well as significant cancer cell selectivity, were found to have the highest anticancer activity in vitro testing, on human colon carcinoma cells.
Source link: https://europepmc.org/article/MED/35740458
Introduction Calotropis procera Dryand is a herb that has been used in folk medicine to treat various illnesses for more than 1500 years. Aims Our aim was to investigate the anti-metastatic effects of phenolics extracted from C. procera cells and in BALB/c mice. Methods 4T1 cells were treated with CphE and quercetin at concentrations that inhibited cell viability by 50%. Mammary fat pads were transplanted into mammary fat pads, delivering 4T1 cells. Tumors were allowed to grow for nine days before beginning with CphE or PBS for a week. CphE suppressed cell viability in vitro by apoptosis induction, as shown by caspase-3 cleavage and total PARP reduction. CphE's anti-invasive cancer treatment by reduction of Cenpf mRNA levels in liver and lung tissues was a strong anti-invasive cancer treatment. Conclusions CphE inhibited 4T1 cell signal pathways, which play a significant role in cell proliferation and invasion.
Source link: https://europepmc.org/article/MED/35676853
Historical Background The leaves of Simarouba glauca can be used as a potential source of anticancer agents in traditional medicine. Attempts have been made to isolate anticancer agents from the leaves of S. glauca's leaves. Human non-small-cell lung cancer A549 cells were tested for anticancer and apoptotic activity by the leaf extract of petroleum ether in human non-small-cell lung cancer A549 cells. Caspase 3 reports indicated that the cell death occurred either through the mitochondrial pathway or the death receptor.
Source link: https://europepmc.org/article/MED/35763625
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